Xiaoming Ju, MD
233 S. Tenth Street, Suite 1028
Philadelphia, PA 19107
(215) 923-4498 fax
Most Recent Peer-reviewed Publications
- The endogenous cell-fate factor dachshund restrains prostate epithelial cell migration via repression of cytokine secretion via a CXCL signaling module
- CCR5 receptor antagonists block metastasis to bone of v-Src oncogene-transformed metastatic prostate cancer cell lines
- Cyclin D1 integrates estrogen-mediated DNA damage repair signaling
- Identification of a cyclin D1 network in prostate cancer that antagonizes epithelial-mesenchymal restraint
- miR-17/20 sensitization of breast cancer cells to chemotherapy-induced apoptosis requires Akt1
MD, Binzhou Medical University, China
MS, PhD, First Hospital, Beijing Medical University, China
Expertise & Research Interests
Dr Ju's research in Kimmel Cancer Center is focused on the molecular mechanisms of refractory and metastatic breast and prostate cancer for therapeutic intervention.
His previous research accomplishments include determination of the in vivo role of Akt1 gene in breast cancer during oncogenesis. The Akt1 gene plays a role in keeping healthy cells alive, it has an overabundance in breast and some other cancer cells. It was unknown whether or not the Akt1 gene actually caused cancer. Ju and his colleagues bred mice that lacked the Akt1 gene with mice that over expressed ErbB2 gene, an oncogene known to cause breast cancer. His study suggested that the Akt1 gene is required for the onset and growth of breast cancer. Furthermore, Akt1 plays an important role in invasion and metastasis of breast cancer, which is the major cause of death in women affected with this disease.
In addition to research on breast cancer, Dr Ju's ongoing research also focuses on the investigation of progression of prostate cancer. He have established novel cancer cell lines through transduction of prostate epithelial cells using oncogene Ha-Ras, c-Myc, v-Src and ErbB2 (NeuT). These new cell lines have been characterized extensively in many cellular processes including cell survival motility; cell proliferation, altered metabolism and angiogenesis. The cells could be studied in immune-competent mice, they grow in mice in a reproducible manner and form metastasis. By faithfully recapitulating the tumor host environment, the new cell lines allow us to conduct further studies based on findings in the transgenic and knockout mice. The aims of their research include revealing the mechanisms by which androgen receptor (AR) function is regulated in prostate cancer cellular growth, and determinating if specific cyclins and cyclin dependent kinase inhibitors (CDKI) are required for initiation and progression of prostate tumors which are induced by different oncogenes.